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PubMed1982

Valproic acid: brain and plasma levels of the drug and its metabolites, anticonvulsant effects and gamma-aminobutyric acid (GABA) metabolism in the mouse.

The slow onset and carry-over effect of valproic acid (VPA) therapy observed in some clinical as well as experimental animal studies have been examined by parallel pharmacokinetic and pharmacological investigations in a mouse model. VPA was rapidly transferred into brain and was cleared from that tissue with rates which exceeded plasma clearance rates. Of several VPA metabolites present in plasma, only one could be found in the brain: 2-propyl-2-pentenoic acid. This metabolite was cleared from plasma and from brain slower than the parent drug. gamma-Aminobutyric acid (GABA) concentrations were increased within 15 min after VPA injection and remained significantly elevated for at least 8 h. A similar time course was found in regard to the increase of the electroconvulsive threshold (maximal seizures) induced by VPA administration. The activity of glutamic acid decarboxylase rose parallel to the elevation of brain GABA levels, whereas the activity of GABA aminotransferase was not affected. Whereas the rapid onset of the effect on electroconvulsive threshold and on GABA metabolism can be explained by the rapid entrance of VPA into brain, the carry-over effects observed correlated with the kinetics of the metabolite 2-propyl-2-pentenoic acid better than with those of VPA due to the persistence of this metabolite in brain.

4-Aminobutyrate Transaminase↗
PubMed1997

Neurotransmission by neurons that use serotonin, noradrenaline, glutamate, glycine, and gamma-aminobutyric acid in the normal and injured spinal cord.

OBJECTIVE: The science of neurotransmission in the normal and injured spinal cord has grown. This is a review of neurotransmission using serotonin, noradrenaline, glutamate, glycine, and gamma-aminobutyric acid. METHODS: The literature on spinal cord neurotransmission and changes that occur with trauma are reviewed. CONCLUSION: Serotonergic and noradrenergic bulbospinal tracts influence interneurons and motor neurons via postsynaptic inhibition. Colocalization of serotonin and thyrotropin-releasing hormone occur in bulbospinal tracts, and reduction in uptake and thyrotropin-releasing hormone immunoreactivity quantitates the degree of injury in chronic spinal cord injury (SCI). Glutamate functions as an excitatory transmitter of some dorsal root afferent neurons and interneurons modulating nociceptive and motor neurons via at least five different receptors. Reactive synaptogenesis occurs after SCI, leading to an increase in the number of excitatory glutamatergic synapses below the level of SCI. gamma-Aminobutyric acid is an inhibitory transmitter of spinal interneurons that functions both pre- and postsynaptically. After SCI, a reduction occurs in the number of inhibitory synapses related to gamma-aminobutyric acid. Glycine is an inhibitory neurotransmitter that functions postsynaptically and also modulates the N-methyl-D-aspartate receptor. After SCI, a reduction in glycine adds to the loss of local inhibition below the SCI.

Animals↗
PubMed1982

Determination of gamma-aminobutyric acid by liquid chromatography with electrochemical detection.

gamma-Aminobutyric acid (GABA) has been determined in rat brain by derivatization with 2,4,6-trinitrobenzenesulfonic acid. The derivative and an internal standard, 2,4,6-trinitrophenyl-delta-aminovaleric acid, are extracted into toluene and separated by reversed-phase chromatography. Electrochemical reduction of these derivatives permits picomole measurements of GABA in microgram amounts of brain tissue.

Animals↗
PubMed1977

Growth hormone release by gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) in the rat.

Effects of gamma-aminobutyric acid (GABA) and gamma-amino-beta-hydroxybutyric acid (GABOB) on growth hormone (GH) release were investigated in the urethaneanesthetized male rat. An intraventricular injection of GABA and L-GABOB but not D-GABOB caused a significant increase in plasma GH. An intravenous injection of L-GABOB, at the dose which had no significant effect on basal plasma GH, remarkably enhanced plasma GH response to pentobarbital. These results suggest that GABA and L-GABOB stimulate GH release possibly via the central nervous system in the rat.

Aminobutyrates↗
PubMed1979

Gamma-aminobutyric-acid deficiency in brain of schizophrenic patients.

Gamma-aminobutyric acid (G.A.B.A.) was measured in the nucleus accumbens and thalamus of brains from patients who had died with schizophrenia or Huntington's chorea (H.C.) and from control subjects. Mean G.A.B.A. content was significantly reduced in both brain areas in schizophrenia and in H.C. Extraneous factors, such as age, interval from death to necropsy, cause of death, and drug use, did not readily explain the observed reduction in brain G.A.B.A. G.A.B.A. deficiency may be a biochemical characteristic of some forms of schizophrenia.

Brain Chemistry↗
PubMed2005

Novel properties of a mouse gamma-aminobutyric acid transporter (GAT4).

We expressed the mouse gamma-aminobutyric acid (GABA) transporter GAT4 (homologous to rat/ human GAT-3) in Xenopus laevis oocytes and examined its functional and pharmacological properties by using electrophysiological and tracer uptake methods. In the coupled mode of transport (Na+/ Cl-/GABA cotransport), there was tight coupling between charge flux and GABA flux across the plasma membrane (2 charges/GABA). Transport was highly temperature-dependent with a temperature coefficient (Q10) of 4.3. The GAT4 turnover rate (1.5 s(-l); -50 mV, 21 degrees C) and temperature dependence suggest physiological turnover rates of 15-20 s(-1). No uncoupled current was observed in the presence of Na+. In the absence of external Na+, GAT4 exhibited two distinct uncoupled currents. (i) A Cl- leak current (ICl(leak)) was observed when Na+ was replaced with choline or tetraethylammonium. The reversal potential of (ICl(leak)) followed the Cl- Nernst potential. (ii) A Li+ leak current (ILi(leak)) was observed when Na+ was replaced with Li+. Both leak currents were inhibited by Na+, and both were temperature-independent (Q10 approximately 1). The two leak modes appeared not to coexist, as Li+ inhibited (ICl(leak)). The results suggest the existence of cation- and anion-selective channel-like pathways in GAT4. Flufenamic acid inhibited GAT4 Na+/Cl-/GABA cotransport, ILi(leak), and ICl(leak), (Ki approximately 30 microM), and the voltage-induced presteady-state charge movements (Ki approximately 440 microM). Flufenamic acid exhibited little or no selectivity for GAT1, GAT2, or GAT3. Sodium and GABA concentration jicroumps revealed that slow Na+ binding to the transporter is followed by rapid GABA-induced translocation of the ligands across the plasma membrane. Thus, Na+ binding and associated conformational changes constitute the rate-limiting steps in the transport cycle.

Animals↗
PubMed1978

Erythrocyte membrane alterations in Huntington disease: effects of gamma-aminobutyric acid.

The interaction of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) with erythrocyte membranes from patients with Huntington disease and normal controls has been studied by electron spin resonance. GABA affects the physical state of erythrocyte membrane proteins in control and Huntington disease differently. In addition, after exposure of spin-labeled Huntington disease erythrocyte membranes to 0.1 mM GABA, the relevant electron spin resonance parameters reflecting the physical state of membrane proteins are indistinguishable from those of untreated control membranes. These findings support the concept that this disease is associated with a generalized membrane defect.

Electron Spin Resonance Spectroscopy↗
PubMed1996

Plasma levels of gamma-aminobutyric acid and panic disorder.

Low levels of gamma-aminobutyric acid (GABA) in plasma have been associated with the presence of mood disorders in patients with major depressive disorder. We examined plasma GABA in patients with panic disorder, a disorder that is often comorbid with major depression, and in a group of control subjects. Patients with panic disorder had plasma GABA levels that did not differ significantly from levels in controls subjects. These data support the specificity of low plasma GABA as a marker for mood disorders.

Adult↗
PubMed1985

gamma-Aminobutyric acid in peripheral tissues.

Significant amounts of gamma-aminobutyric acid (GABA), an endogenous amino acid, are present in mammalian peripheral tissues. This finding led to the suggestion that GABA may act as a neurotransmitter in the peripheral nervous system as it does in the central nervous system. This review deals with recent identification of GABA in the autonomic nervous system and the possible functional role of GABA in neuronal and non-neuronal tissues. The identification of GABA in the autonomic nervous system has paved the way for new approaches in pharmacological investigations.

Animals↗
PubMed1988

Experimental study on central effects of carboxyethyl-gamma-aminobutyric acid (CEGABA).

The central effects of carboxyethyl-gamma-aminobutyric acid (CEGABA) have been studied both in rabbits and in the guinea pig myoclonus model. This drug caused EEG synchronization and behavioural sedation both after intravenous (i.v.) and intracerebroventricular (i.c.v.) administration in a dose-dependent manner, in rabbits. CEGABA showed a protective action against myoclonus induced by means of L-5-HTP in young guinea pigs. These data substantiate the hypothesis that CEGABA is a drug active on the central nervous system and probably exerts its action by strengthening cortical inhibition and/or directly acting on lower brainstem.

5-Hydroxytryptophan↗
PubMed1981

gamma-Aminobutyric acid concentration in cerebrospinal fluid in schizophrenia.

gamma-Aminobutyric acid (GABA) concentration was determined in cerebrospinal fluid (CSF) of acute and chronic schizophrenic patients, in persons with psycho-organic or personality disorders, and in nonpsychiatric controls. The mean CSF GABA level in the chronic schizophrenic patients was found to be significantly higher than in any of the other groups. No other statistically significant differences were found. Statistical analysis revealed that the elevated CSF GABA concentration in the chronic schizophrenic patients was unlikely to be caused by medication. These results are interpreted as evidence for possible primary or secondary GABAergic overactivity in the brain in chronic schizophrenia.

Acute Disease↗
PubMed1981

gamma-Aminobutyric acid and benzodiazepine receptors: copurification and characterization.

gamma-Aminobutyric acid (GABA) and benzodiazepine receptors have been solubilized and purified by procedures such as gel filtration, ion-exchange, lectin, and affinity chromatographies. All of these procedures enhance the specific activity of each receptor to a similar extent. The drug specificities of [3H]muscimol and [3H]flunitrazepam binding sites are the same after extensive purification by affinity chromatography compared to the membrane bound and initially solubilized receptors. GABA and chloride stimulation of benzodiazepine binding is retained in pure receptors. Two bands are covalently labeled with [3H]flunitrazepam after ultraviolet irradiation of the purified receptor. The persistent association of GABA, benzodiazepine, and chloride recognition sites after extensive purification suggests that they may be part of a single macromolecular complex.

Animals↗
PubMed1982

gamma-Aminobutyric acid system in cardiovascular and cerebrovascular function.

gamma-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the vertebrate CNS. Recent experiments have begun to delineate the roles of GABA neurons in control of both central sympathetic and parasympathetic outflows to the heart and vasculature. It is suggested that incoordination in these regions resulting from inadequate function of GABA neurons could lead to cardiac arrhythmias and large fluctuations in blood pressure that would predispose to cardiac and vascular damage. A role for GABA in cerebrovascular function is supported by the observation that specific GABA receptors and GABA-related enzymes are associated with cerebral blood vessels. It is suggested that a non-neural, indigenous GABA system in cerebral blood vessels is involved in the control of cerebrovascular tone. GABA probably plays an important role in the complex processes involved in normal regulation of cerebral circulation and its dysfunction.

4-Aminobutyrate Transaminase↗
PubMed1989

Active transport of gamma-aminobutyric acid and glycine into synaptic vesicles.

Although gamma-aminobutyric acid (GABA) and glycine are recognized as major amino acid inhibitory neurotransmitters in the central nervous system, their storage is poorly understood. In this study we have characterized vesicular GABA and glycine uptakes in the cerebrum and spinal cord, respectively. We present evidence that GABA and glycine are each taken up into isolated synaptic vesicles in an ATP-dependent manner and that the uptake is driven by an electrochemical proton gradient. Uptake for both amino acids exhibited kinetics with low affinity (Km in the millimolar range) similar to vesicular glutamate uptake. The ATP-dependent GABA uptake was not inhibited by the putative amino acid neurotransmitters glycine, taurine, glutamate, or aspartate or by GABA analogs, agonists, and antagonists. Similarly, ATP-dependent glycine uptake was hardly affected by GABA, taurine, glutamate, or aspartate or by glycine analogs or antagonists. The GABA uptake was not affected by chloride, which is in contrast to the uptake of the excitatory neurotransmitter glutamate, whereas the glycine uptake was slightly stimulated by low concentrations of chloride. Tissue distribution studies indicate that the vesicular uptake systems for GABA, glycine, and glutamate are distributed in different proportions in the cerebrum and spinal cord. These results suggest that the vesicular uptake systems for GABA, glycine, and glutamate are distinct from each other.

Adenosine Triphosphatases↗
PubMed1975

Autoradiographic localization of 3H-gamma-aminobutyric acid in the medial hypothalamus.

Tritium labelled gamma-aminobutyric acid (3H-GABA) was infused into the third ventricle of rats with normal or deafferented hypothalamus and the distribution of the label was studied by light and electron microscopic autoradiography. In control as well as deafferented hypothalamus a few neurones accumulated radioactivity, while the majority was unlabelled. Characteristic clusters and rows of silver grains were observed in the neuropil of several regions probably indicating labelled cell processes and terminal axons. Electron microscopy showed that at least some of the clusters were over axon terminals with synaptic vesicles. 3H-GABA accumulated also in the ependyma and glial elements. The results suggest that in the medial hypothalamus there is a preferential uptake of GABA in some neurones and nerve fibers; at least some of these are hypothalamic interneurones. This supports the hypothesis that some hypothalamic neurones and nerve endings may use GABA as a transmitter.

Alanine↗
PubMed1981

Concurrent acetylcholinesterase staining and gamma-aminobutyric acid uptake of cortical neurons in culture.

Gamma-aminobutyric acid (GABA) uptake and acetylcholinesterase (AChE) content were demonstrated concurrently in cortical neurons grown in tissue culture. Positive reactions either for GABA uptake or for AChE content were encountered in pyramidal and stellate, as well as spindle-shaped neurons. Neither reaction was confined to a specific morphological subtype. Nearly half the neurons were negative for either reaction. Most of the remaining neurons were positive only for GABA or only for AChE. However, a subpopulation of neurons showed not only a high AChE content, but also an avid GABA uptake. Thus, four types of neurons could be identified on the basis of these two reactions. The high AChE content in some of the cortical neurons that also showed GABA uptake indicates that there are at least two distinct types of GABAergic neurons.

Acetylcholinesterase↗
PubMed1983

Gamma-aminobutyric acid (GABA) in cerebrospinal fluid.

Levels of gamma-aminobutyric acid (GABA) in cerebrospinal fluid (CSF) were measured by radioreceptor assay (RRA) in 25 normal controls and in 121 patients with various central nervous system disorders. CSF-GABA levels could be measured down to 5 pmoles/ml reliably by this assay. In normal controls, the mean (+/- SEM) GABA level in CSF was 127 +/- 5.2 pmoles/ml. There was no correlation between age, sex and the CSF-GABA level in normal controls. The lowest CSF-GABA level, which was 60 +/- 6.0 pmoles/ml, was observed in alcoholic patients suffering from cerebellar ataxia. The CSF-GABA levels were quite low in patients with Alzheimer's disease, late cortical cerebellar atrophy, neuro-Behçet's syndrome, olivopontocerebellar atrophy, Huntington's chorea, Parkinson's disease and cerebral hemorrhage. On the other hand, the CSF-GABA levels of meningitis patients were significantly increased. These findings suggest that measuring the CSF-GABA level is quite beneficial in the diagnosis and pathophysiological determinations of some diseases.

Adult↗
PubMed1995

Levels of gamma-aminobutyric acid in cerebrospinal fluid and plasma during alcohol withdrawal.

Aminobutyric acid (GABA) is implicated in the biochemical pathophysiology of alcohol intoxication, dependence and withdrawal. We therefore measured GABA in both cerebrospinal fluid (CSF) and plasma from 14 male alcohol-dependent patients during acute alcohol withdrawal (day 1) and again after 21 days of inpatient treatment (day 21). Plasma GABA levels on admission correlated with indices of liver function. When corrected for differences in liver function, plasma levels of GABA levels on day 1 were significantly higher than on day 21. CSF GABA concentrations were also significantly higher during withdrawal compared with concentrations after 3 weeks of abstinence. The change in plasma GABA levels correlated significantly with the change in CSF GABA levels, although there was no correlation between plasma and CSF levels at either time. These findings demonstrate that changes in CSF GABA may be reflected in plasma GABA, and they highlight the potential importance of the GABA system in alcohol dependence and withdrawal.

Adult↗